SUBVERTING LYMPH-NODE TRAFFICKING BY TREATMENT WITH THE MEL-14 MONOCLONAL-ANTIBODY TO L-SELECTIN DOES NOT PREVENT AN EFFECTIVE HOST RESPONSE TO SENDAI VIRUS

A single 250-mu g dose of the Mel-14 mAb to L-selectin greatly diminis hed the extent of L-selectin expression on lymphocytes and decreased ( 60 to 90%) the massive cellular recruitment to the cervical and medias tinal lymph nodes that follows intranasal infection of naive C57BL/6 m ice with Sendai virus. The numbers of CD8(+) CTL precursors in the med iastinal lymph nodes were considerably reduced on day 7, when compared with virus-infected mice given a control rat IgG2a, but potent CTL ef fecters were present in the lungs of both groups by day 10 after infec tion, and the overall magnitude of CTL precursor generation was not ob viously compromised. The early dominance of Sendai virus-specific IgM Ab-forming cells was prolonged in the Mel-14-treated mice, whereas pla sma cells producing virus-specific IgA were abnormally prominent in th e lymph nodes but not in the spleen. The kinetics of virus-specific Ab -forming cells generation and the serum Ab response for the various Ig G isotypes were also delayed, Thus, though L-selectin is clearly impor tant for the localization of naive lymphocytes to regional lymph nodes , the Mel-14-treated mouse san still deal effectively with a virus tha t causes productive infection only in the respiratory tract. The splee n, where L-selectin does not determine lymphocyte trafficking, is a ma jor site for the compensatory T cell and B cell responses.